ArticleFrontiers in aging neuroscience2019
Cre-Dependent Optogenetic Transgenic Mice Without Early Age-Related Hearing Loss.
Article in Frontiers in aging neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 16 citations in OpenAlex.
- Developmental overproduction of cortical superficial neurons impairs adult auditory cortical processing.Scientific reports · 2025Article
- Sst- and Vip-Cre mouse lines without age-related hearing loss.bioRxiv : the preprint server for biology · 2024Article
- Experimentally unsupervised deconvolution for light-sheet microscopy with propagation-invariant beams.Light, science & applications · 2022Article
- Effects of optogenetic stimulation of basal forebrain parvalbumin neurons on Alzheimer's disease pathology.Scientific reports · 2020Article
- Generation of a ChATHearing research · 2020Article
- Biased M1-muscarinic-receptor-mutant mice inform the design of next-generation drugs.Nature chemical biology · 2020Article
- State-dependent brainstem ensemble dynamics and their interactions with hippocampus across sleep states.eLife · 2020Article
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2 authors at 1 institution in 1 country.
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Abstract
With the advent of recent genetic technologies for mice, it is now feasible to investigate the circuit mechanisms of brain functions in an unprecedented manner. Although transgenic mice are commonly used on C57BL/6J (C57) background, hearing research has typically relied on different genetic backgrounds, such as CBA/Ca or CBA due to the genetic defect of C57 mice for early age-related hearing loss. This limits the utilization of available genetic resources for hearing research. Here we report congenic (>F10) Cre-dependent channelrhodopsin2 (ChR2) mice on CBA/Ca background. By crossing this line with Cre-driver mice on C57 background, F1 hybrids restored the hearing deficit of C57 mice. We also found a linear relationship between aging and hearing loss, with progression rates varied depending on genetic backgrounds (3.39 dB/month for C57; 0.82 dB/month for F1 hybrid). We further demonstrate that this approach allows to express ChR2 in a specific type of inhibitory neurons in the auditory cortex and that they can be identified within a simultaneously recorded population of neurons in awake mice. Thus, our Cre-dependent optogenetic transgenic mice on CBA/Ca background are a valuable tool to investigate the circuit mechanisms of hearing across lifespan.
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